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Notes: Abstract: An in vitro model of ischemia was obtained by subjectingPC12 cells differentiated with nerve growth factor to a combination of glucosedeprivation plus anoxia. Immediately after the ischemic period, the proteinsynthesis rate was significantly inhibited (80%) and western blots of cellextracts revealed a significant accumulation of phosphorylated eukaryoticinitiation factor 2, α subunit, eIF2(αP) (42%). Upon recovery,eIF2(αP) levels returned to control values after 30 min, whereas proteinsynthesis was still partially inhibited (33%) and reached almost controlvalues within 2 h. The activities of the mammalian eIF2α kinases,double-stranded RNA-activated protein kinase, mammalian GCN2 homologue, andendoplasmic reticulum-resident kinase, were determined. None of theeIF2α kinases studied showed increased activity in ischemic cells ascompared with controls. Exposure of cells to cell-permeable inhibitors ofprotein phosphatases 1 and 2A, calyculin A or tautomycin, induced dose- andtime-dependent accumulation of eIF2(αP), mimicking an ischemic effect.Protein phosphatase activity, as measured with [32P]phosphorylasea as a substrate, diminished during ischemia and returned to controllevels upon 30-min recovery. In addition, the rate of eIF2(αP)dephosphorylation was significantly lower in ischemic cells, paralleling boththe greatest translational inhibition and the highest eIF2(αP) levels.The endogenous phosphatase activity from control and ischemic extracts showeddifferent sensitivity to inhibitor 2 and fostriecin in in vitro assays,inhibitor-2 effect in ischemic cells being lower than in control cells.Together these results indicate that an eIF2α phosphatase, probablyprotein phosphatase 1, is implicated in the ischemia-induced eIF2(αP)accumulation in PC12 cells.

Notes: Summary.— Biopsies from 10 patients with lichen amyloidosus were investigated histochemically with special reference to the epidermal changes. The number of dopa-positive melanocytes was markedly decreased in the epidermis overlying the amyloid deposits, indicating that melanocytes are also involved and probably destroyed by the disease process. No increase in lysosomal enzyme activity could be detected in epidermal cells undergoing degeneration or in the epidermis immediately above the amyloid deposits. Respiratory enzyme activity was moderately reduced in the epidermis overlying the amyloid deposits. These histochcmical findings confirm that the epidermis is likely to be involved in the histopathogenesis of lichen amyloidosus. It is suggested that, prior to the deposition of amyloid, a specific cellular tolerance may develop to the presence of necrotic epidermal cells in the region of the dermo-epidermal junction.

Notes: A 17-year-old female is described who presented with an unusual form of macular amyloidosis which closely simulated naevoid hyperpigmentation. Electron microscopy was necessary to provide specific identification of the sparse deposits of amyloid.

Notes: A Monte Carlo analysis of bipolar transport and voltage fluctuations in a p+-Si/n-Si0.7Ge0.3 heterojunction and in a p+n Si homojunction under different operation regimes is presented. Comparison of the spectral density of voltage fluctuations at low frequency, SV(x,0), between both structures reveals the strong effect of the SiGe layer on the noise behavior in the heterojunction. Alloy scattering hinders the electron mobility enhancement expected from the removal of valley degeneracy in the SiGe layer. Despite this mobility reduction, the greater accumulation of carriers in the low-doped region supported by the valence band discontinuity reduce SV(x,0) in the heterojunction for a given average voltage. This study also reveals the impact of hot carriers on noise performance in the quasisaturation regime of both diodes. © 2000 American Institute of Physics.

Notes: Translational repression induced during reperfusion of the ischaemic brain is significantly attenuated by ischaemic preconditioning. The present work was undertaken to identify the components of the translational machinery involved and to determine whether translational attenuation selectively modifies protein expression patterns during reperfusion. Wistar rats were preconditioned by 5-min sublethal ischaemia and 2 days later, 30-min lethal ischaemia was induced. Several parameters were studied after lethal ischaemia and reperfusion in rats with and without acquired ischaemic tolerance (IT). The phosphorylation pattern of the α subunit of eukaryotic initiation factor 2 (eIF2) in rats with IT was exactly the same as in rats without IT, reaching a peak after 30 min reperfusion and returning to control values within 4 h in both the cortex and hippocampus. The levels of phosphorylated eIF4E-binding protein after lethal ischaemia and eIF4E at 30 min reperfusion were higher in rats with IT, notably in the hippocampus. eIF4G levels diminished slightly after ischaemia and reperfusion, paralleling calpain-mediated α-spectrin proteolysis in rats with and without IT, but they did not show any further decrease after 30 min reperfusion in rats with IT. The phosphorylated levels of eIF4G, phosphatidylinositol 3-kinase-protein B (Akt) and extracellular signal-regulated kinases (ERKs) were very low after lethal ischaemia and increased following reperfusion. Ischaemic preconditioning did not modify the observed changes in eIF4G phosphorylation. All these results support that translation attenuation may occur through multiple targets. The levels of the glucose-regulated protein (78 kDa) remained unchanged in rats with and without IT. Conversely, our data establish a novel finding that ischaemia induces strong translation of growth arrest and DNA damage protein 34 (GADD34) after 4 h of reperfusion. GADD34 protein was slightly up-regulated after preconditioning, besides, as in rats without IT, GADD34 levels underwent a further clear-cut increase during reperfusion, this time as earlier as 30 min and coincident with translation attenuation.